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A 3-year trial involving persons with a family history of dementia showed no differences in cognitive change or brain MRI outcomes between the MIND diet, designed for neuroprotection, and a control diet.

Age-related cognitive decline is a well-known phenomenon after age 65 but little is known about earlier changes and prior studies are based on relatively small samples. We investigated the impact of age on cognitive decline in the largest population sample to date including young to old adults. Between 100,352 and 468,534 participants aged 38-73 years from UK Biobank completed at least one of seven self-administered cognitive functioning tests: prospective memory (PM), pairs matching (Pairs), fluid intelligence (FI), reaction time (RT), symbol digit substitution, trail making A and B. Up to 26,005 participants completed at least one of two follow-up assessments of PM, Pairs, FI and RT. Multivariable regression models examined the association between age (<45[reference], 45-49, 50-54, 55-59, 60-64, 65+) and cognition scores at baseline. Mixed models estimated the impact of age on cognitive decline over follow-up (~5.1 years). FI was higher between ages 50 and 64 and lower at 65+ compared to <45 at baseline. Performance on all other baseline tests was lower with older age: with increasing age category, difference in test scores ranged from 2.5 to 7.8%(P<0.0001). Compared to <45 at baseline, RT and Pairs performance declined faster across all older age cohorts (3.0 and 1.2% change, respectively, with increasing age category, P<0.0001). Cross-sectional results yielded 8 to 12-fold higher differences in RT and Pairs with age compared to longitudinal results. Our findings suggest that declines in cognitive abilities <65 are small. The cross-sectional differences in cognition scores for middle to older adult years may be due in part to age cohort effects.

Introduction: Non-pharmacological treatments (NPTs) have the potential to improve meaningful outcomes for older people at risk of, or living with dementia, but research often lacks methodological rigor and continues to produce mixed results.Methods: In the current position paper, experts in NPT research have specified treatment targets, aims, and ingredients using an umbrella framework, the Rehabilitation Treatment Specification System.Results: Experts provided a snapshot and an authoritative summary of the evidence for different NPTs based on the best synthesis efforts, identified main gaps in knowledge and relevant barriers, and provided directions for future research. Experts in trial methodology provide best practice principles and recommendations for those working in this area, underscoring the importance of prespecified protocols.Discussion: We conclude that the evidence strongly supports various NPTs in relation to their primary targets, and discuss opportunities and challenges associated with a unifying theoretical framework to guide future efforts in this area.

Introduction Higher brain tocopherol levels have been associated with lower levels of Alzheimer's disease (AD) neuropathology; however, the underlying mechanisms are unclear. Methods We studied the relations of α‐ and γ‐tocopherol brain levels to microglia density in 113 deceased participants from the Memory and Aging Project. We used linear regression analyses to examine associations between tocopherol levels and microglia densities in a basic model adjusted for age, sex, education, apolipoprotein E (APOE)ε4 genotype (any ε4 allele vs. none) , and post‐mortem time interval, and a second model additionally adjusted for total amyloid load and neurofibrillary tangle severity. Results Higher α‐ and γ‐tocopherol levels were associated with lower total and activated microglia density in cortical but not in subcortical brain regions. The association between cortical α‐tocopherol and total microglia density remained statistically significant after adjusting for AD neuropathology. Discussion These results suggest that the relation between tocopherols and AD might be partly explained by the alleviating effects of tocopherols on microglia activation.

Cortical iron has been shown to be elevated in Alzheimer’s disease (AD), but the impact of the directly measured iron on the clinical syndrome has not been assessed. We investigated the association between post-mortem iron levels with the clinical and pathological diagnosis of AD, its severity, and the rate of cognitive decline in the 12 years prior to death in subjects from the Memory and Aging Project (n = 209). Iron was elevated (β [SE] = 9.7 [2.6]; P = 3.0 × 10−4) in the inferior temporal cortex only in subjects who were diagnosed with clinical AD during life and had a diagnosis of AD confirmed post-mortem by standardized criteria. Although iron was weakly associated with the extent of proteinopathy in tissue with AD neuropathology, it was strongly associated with the rate of cognitive decline (e.g., global cognition: β [SE] = -0.040 [0.005], P = 1.6 × 10−14). Thus, cortical iron might act to propel cognitive deterioration upon the underlying proteinopathy of AD, possibly by inducing oxidative stress or ferroptotic cell death, or may be related to an inflammatory response.

The relationship between smoking status and incident Alzheimer’s disease (AD) was investigated in a random stratified sample of a biracial community in Chicago. Analyses are based on 1,064 persons (of 1,134 evaluated) who had data on smoking status, disease incidence, and key covariates such as apolipoprotein allele status. During a mean of about 4 years of follow-up, 170 persons met criteria for incident AD. Current smoking was associated with increased risk of incident AD (OR = 3.4, 95% CI = 1.4–8.0) compared to persons who never smoked. There was no apparent increase in risk of AD for former smokers compared to persons who never smoked (OR = 0.9, 95% CI = 0.5–1.7). Apolipoprotein E allele status modified this association in that former smokers with a υ4 allele were less likely to develop AD (p = 0.04) than those who never smoked. Former smokers also appeared to have a reduced risk of developing AD as their pack-years of smoking increased (p = 0.02)such that the odds of developing AD increased by 50% for every 10 years of smoking cessation (OR = 1.3, CI = 0.9–1.7). The results suggest that older people who currently smoke are more likely to develop AD compared to those who never smoked; the relation between those who used to smoke but quit and the risk of AD is complex and requires further research.

Background: Strawberries have been identified to have antioxidant and anti-inflammatory properties that improve neuronal function and cognition, mostly in animal studies. It is unknown if the consumption of strawberries or related bioactives may reduce the risk of Alzheimer’s dementia risk. Material and Methods: The study was conducted in 925 participants, aged 58–98 years of the Rush Memory and Aging Project. Participants were dementia-free at baseline, completed a food frequency questionnaire, and had at least two annual neurological evaluations. The diagnosis of Alzheimer’s dementia was based on structured clinical neurological examination and standardized diagnostic criteria. The association of strawberry intake and incident Alzheimer’s dementia was analyzed using proportional hazard models adjusted for age, sex, education, physical activity, participation in cognitive activities, APOE-ɛ4 genotype, dietary intake of other fruits, and total calorie intake. Results: A total of 245 participants developed Alzheimer’s dementia over the mean follow-up of 6.7 (±3.6) years. Higher strawberry intake was associated with reduced risk of Alzheimer’s dementia (HR = 0.76, 95% CI: 0.60–0.96). In separate adjusted models, highest vs. lowest quartile intakes of Vitamin C (HR = 0.64, 95% CI: 0.45, 0.92), Pelargonidin (0.63, 95% CI: 0.43, 0.92), total anthocyanidins (0.69, 95% CI: 0.48, 0.99), and total flavonoids (0.67, 95% CI: 0.46, 0.98) were each associated with lower Alzheimer’s dementia risk. These associations remained after further adjustment for cardiovascular conditions. Conclusion: Consumption of strawberries and foods rich in vitamin C, pelargonidin, anthocyanidins, and total flavonoids may reduce the risk of Alzheimer’s dementia.

Clinical evidence points to the premise that caffeine may benefit cognition, but whether these findings extend to real life settings and amidst factors that impact caffeine metabolism is unclear. The aim of this study was to investigate the impact of recent caffeine drinking on cognitive ability while additionally accounting for lifestyle and genetic factors that impact caffeine metabolism. We included up to 434,900 UK Biobank participants aged 37–73 years, recruited in 2006–2010, who provided biological samples and completed touchscreen questionnaires regarding sociodemographic factors, medical history, lifestyle, and diet. Recent caffeine drinking (yes/no in the last hour) was recorded during a physical assessment. Participants completed at least one of four self-administered cognitive function tests using the touchscreen system: prospective memory (PM), pairs matching (Pairs), fluid intelligence (FI), and reaction time (RT). Multivariable regressions were used to examine the association between recent caffeine drinking and cognition test scores. We also tested interactions between recent caffeine drinking and a genetic caffeine-metabolism score (CMS) on cognitive function. Among white participants, recent caffeine drinking was associated with higher performance on RT but lower performance on FI, Pairs, and PM (p ≤ 0.004). Similar directions of associations for FI (p = 0.09), Pairs (p = 0.03), and PM (p = 0.34) were observed among non-white participants. No significant and consistent effect modification by age, sex, smoking, test time, habitual caffeine intake, or CMS was observed. Caffeine consumed shortly before tasks requiring shorter reaction times may improve task performance. Potential impairments in memory and reasoning tasks with recent caffeine drinking warrant further study.

Background U.S. POINTER was a multisite randomized controlled trial testing the impact of multidomain lifestyle intervention on cognitive function in cognitively unimpaired older adults at risk for cognitive decline and dementia. Inspired by the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER), the study aimed to assess the generalizability of FINGER's positive cognitive findings in a diverse and representative U.S. cohort. Method The U.S. POINTER interventions were modeled on FINGER, targeting physical activity, nutrition, cognitive/social challenge, and cardiometabolic risk management. Additional goals included (1) delivering the intervention within the community, (2) collaborating with community partners (Alzheimer's Association, community exercise facilities) to ensure/test intervention sustainability, (3) incorporating objective adherence metrics to permit responder analyses, (4) adapting the MIND diet, and (5) introducing a cognitive training program with greater potential for participant adoption. The interventions were designed and implemented using a cognitive‐behavioral framework and theory driven self‐motivation tools. Intervention fidelity was centrally monitored through data‐driven reports and annual site visits. Results U.S. POINTER interventions included two arms, both targeting multidomain lifestyle modification but differing in intensity and accountability. Following the baseline assessment, participants were randomized to the Structured (STR) or Self‐Guided (SG) arm. The STR intervention included 38 group sessions, a structured exercise prescription using community facilities, a nutrition program modeled on the MIND diet, BrainHQ computerized cognitive training, regular cognitive/social challenge, and frequent cardiometabolic health monitoring. The SG intervention included six facilitated group sessions, general health education across all intervention domains, and gift cards to support participants’ chosen health behaviors. Adherence was tracked using objective and self‐report metrics, with central monitoring to ensure consistent implementation across sites. Conclusion U.S. POINTER expands upon FINGER with modifications aimed at improving intervention uptake and accountability in a U.S. cohort. The study design will permit extensive analyses of adherence as it relates to cognitive response. Findings could have significant implications for future trials and for public health programs aimed at reducing Alzheimer's disease and dementia risk in older U.S. adults.

Adherence to Mediterranean-DASH Diet Intervention for Neurodegenerative Delay (MIND) may lower the risk of dementia by impacting immunity and cholesterol, which are pathways also implicated by genome-wide association studies of Alzheimer’s Dementia (AD). We examined whether adherence to the MIND diet could modify the association of genetic risk for AD with incident dementia. We used three ongoing US cohorts: Chicago Health and Aging Project (CHAP, n = 2449), Rush Memory and Aging Project (MAP, n = 725), and Women’s Health Initiative Memory Study (WHIMS, n = 5308). Diagnosis of dementia was based on clinical neurological examination and standardized criteria. Repeated measures of global cognitive function were available in MAP and CHAP. Self-reported adherence to MIND was estimated using food-frequency questionnaires. Global and pathway-specific genetic scores (GS) for AD were derived. Cox proportional hazard, logistic regression, and mixed models were used to examine associations of MIND, GS, and GS-MIND interactions with incident dementia and cognitive decline. Higher adherence to MIND and lower GS were associated with a lower risk of dementia in MAP and WHIMS and a slower rate of cognitive decline in MAP (p < 0.05). MIND or GS were not associated with incident dementia or cognitive decline in CHAP. No gene–diet interaction was replicated across cohorts. Genetic risk and MIND adherence are independently associated with dementia among older US men and women.